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    Home > Active Ingredient News > Study of Nervous System > Pan Bingxing's team made a series of important advances in the study of neural loop mechanisms caused by stress and excessive anxiety.

    Pan Bingxing's team made a series of important advances in the study of neural loop mechanisms caused by stress and excessive anxiety.

    • Last Update: 2020-07-21
    • Source: Internet
    • Author: User
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    In recent decades, the rapid development of social economy has greatly improved people's living standards.but along with it, people's life and work pressure is also increasing.as we all know, moderate stress (also known as stress) can guide the body to establish effective coping strategies to enhance the individual's survival ability; however, long-term or excessive stress exposure, especially the inevitable high pressure of life and work, is an important social environmental factor leading to anxiety disorder / depression and other important mental diseases. According to the latest mental health survey data in 2019, the incidence rate of anxiety disorders is the highest among mental disorders. The lifetime prevalence rate ofis as high as 7.6%. However, the current treatment methods and corresponding efficacy of stress related mental disorders are far from satisfactory.to fully elucidate the brain mechanism of stress-induced anxiety disorder is expected to provide a potential direction for exploring new disease treatment strategies.located in the deep temporal lobe, amygdala is a core brain area that expresses and regulates emotions, and plays an important role in the regulation of stress response.the amygdala has extensive structural and functional connections with the cerebral cortex and many subcortical areas.under physiological conditions, amygdala is strongly regulated by top-down inhibition originating from prefrontal cortex (PFC), thus avoiding excessive activation of amygdala and inappropriate negative emotions.on the contrary, prolonged stress exposure significantly weakens the regulation of amygdala by prefrontal cortex, which leads to abnormal activation of amygdala and excessive anxiety.interestingly, although the projection neurons (PN) in the amygdala are intermingled in spatial distribution, their structural and functional connections with other brain regions show obvious heterogeneity: that is, different PNS have relatively specific projection targets and play different or even opposite functions.how chronic stress affects the prefrontal cortex's innervation of these neurons with different functions, and how these effects participate in stress-induced excessive anxiety remains unknown.on May 6, 2020, the research group of Professor Pan Bingxing of the Institute of life sciences of Nanchang University (doctoral students Liu Weizhu and associate researcher Zhang Wenhua are the co first authors of the paper, and Professor Pan Bingxing is the corresponding author) published the Title "identification of a prefrontal cortex to amygdala pathway for chronic stress induced" in nature communications Chronic stress exposure can selectively regulate the control of prefrontal cortex to specific groups of amygdala neurons, and eventually cause excessive anxiety.they first found that chronic restraint stress significantly weakened the inhibitory regulation of the dorsomedial prefrontal cortex (dmPFC) on PN in the basolateral amygdala (BLA).this weakening effect is due to the enhancement of excitatory transmission of dmPFC to blapn; on the contrary, it has no significant effect on feedforward inhibition induced by dmPFC input on blapn, which leads to the shift of E / I balance dominated by dmPFC to the excitatory side of blapn, resulting in the de inhibition effect.interestingly, the de inhibition effect of chronic stress on blapn mainly occurred in the dmPFC pathway, but not in the ventromedial prefrontal cortex (vmPFC) and ventral hippocampus (vhpc).the researchers further explored how chronic stress affects the regulation of dmPFC on different groups of PN in bla.the results showed that chronic stress mainly de inhibited the PN (dmPFC → BLA PNS) receiving dmPFC unidirectional input in bla, but had an interactive projection with dmPFC (dmPFC) A kind of This differential regulation was mainly due to the selective enhancement of presynaptic glutamate transmitter release by dmPFC. in order to clarify the effect of chronic stress on dmPFC → bla The potential relationship between presynaptic glutamate neurotransmitter release and excessive anxiety in PNS was further explored. The potential correlation between presynaptic neurotransmitter release level of dmpfc-bla loop and anxiety like behavior in normal and chronic stressed mice was further explored. The results showed that the anxiety inducing effect of chronic stress was closely related to the up regulation of presynaptic glutamate transmitter release of dmPFC → BLA PNS. finally, in order to clarify whether there is a causal effect in this relationship, researchers have found a photogenetic stimulation method that can specifically reverse chronic stress and enhance the release of presynaptic glutamate transmitter of dmPFC → BLA PNS through a series of experiments; using this method, the light stimulation intervention on stressed mice can effectively reverse the anxiety induced effect of chronic stress. it is particularly important that this reversal effect may exist for a long time. in conclusion, this study comprehensively explored the remodeling effect of chronic stress on dmpfc-bla circuit and its potential pathological significance, which provided important preclinical evidence for precise intervention of stress-related mental disorders. it is reported that this is one of the important achievements made by Professor Pan Bingxing's team in recent years, focusing on "the amygdala mechanism of excessive anxiety caused by chronic stress". in 2019, their team published two consecutive research papers in biological psychology, a well-known Journal of psychiatry, to deeply study the loop mechanism of chronic stress remodeling the structure and function of amygdala neurons. the results showed that chronic stress specifically downregulated the function of small conductance calcium dependent potassium channels (SKCa) projecting to the ventral hippocampal neurons in the BLA, resulting in the overactivation of the BLA vhpc loop, and then increased the anxiety like behavior of mice (Biological Psychology, 2019, 85:812-828; associate researcher Zhang Wenhua is the first author of the paper, and Professor Pan Bingxing is the corresponding author). in addition, they also found that chronic stress can cause extensive dendritic growth in different groups of PN in bla, but interestingly, the concomitant dendritic spines proliferation only appeared in the BLA neurons projecting to the hippocampus (not prefrontal cortex or nucleus accumbens), resulting in increased glutamatergic synaptic input. this differential regulation based on neuronal projection targets is closely related to the anxiety inducing effect of stress (biological psychology, 2019, 85:189-201; associate researcher Zhang Junyu and doctoral candidate Liu taohui are co authors of the paper, and Professor Pan Bingxing is the communication author). a series of studies have shown that chronic stress causes abnormal structure and function of the dmPFC bla vhpc loop in the dorsomedial prefrontal cortex, basolateral amygdala and ventral hippocampus (dmPFC bla vhpc), which plays an important role in impairing the emotional function of the brain. original link: plate maker: Ke
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